4.6 Article

Changes in blood pressure during treatment with the tyrosine kinase inhibitor lenvatinib

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CLINICAL KIDNEY JOURNAL
卷 14, 期 1, 页码 325-331

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OXFORD UNIV PRESS
DOI: 10.1093/ckj/sfaa137

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ambulatory blood pressure monitoring; blood pressure; lenvatinib; tyrosine kinase inhibitor; urinary sodium excretion

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Lenvatinib treatment initiation may lead to hypertension and fluid retention. Reduced urinary sodium excretion in the early stages of treatment could be a contributing factor to fluid retention and hypertension.
Background: Within the class of tyrosine kinase inhibitors (TKIs), which are used for the treatment of numerous advanced cancers, lenvatinib is associated with a higher prevalence of hypertension (HT) compared with other TKIs. In this study, we investigated the effect of lenvatinib on blood pressure (BP) and associated factors. Methods: This single-centre, retrospective observational study included 25 consecutive patients treated with lenvatinib for unresectable hepatocellular carcinoma from April 2018 to December 2018 at the study institution. We assessed changes in BP using ambulatory BP monitoring, urinary sodium excretion, kidney function, use of antihypertensive agents and diuretics, and fluid retention following treatment initiation with lenvatinib. Results: At 1week after treatment initiation, the mean BP and the percentage of patients with riser pattern significantly increased compared with those at the baseline. Although there were no significant changes at 1 week, urinary sodium excretion (153.451.7 and 112.5 +/- 65.0 mEq/day at 1 and 3 weeks, respectively, P<0.05) and estimated glomerular filtration rate significantly decreased and the number of patients with fluid retention increased at 3 weeks. Furthermore, patients with fluid retention had significantly higher BP or required more intensive BP treatment compared with those without fluid retention. Conclusions: Lenvatinib might lead to HT without fluid retention soon after the initiation of treatment, subsequently leading to a reduction in urinary sodium excretion, thereby contributing to a rise in BP by fluid retention.

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